Honda Yoko, Honda Shuji
Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan.
Ann N Y Acad Sci. 2002 Apr;959:466-74. doi: 10.1111/j.1749-6632.2002.tb02117.x.
The free radical theory of aging proposes that oxidative stress is one of the determinants of an organism's life span. In Caenorhabditis elegans, genetic or environmental changes have been shown to modulate life span. Here we discuss whether changes in the generation and destruction of free radicals are implicated in these life span modulations. Changes in culture oxygen concentrations that are considered to reflect free radical generation perturb the life span. The life spans under high and low oxygen concentrations were shorter and longer, respectively, than those under normoxic conditions. Short-term exposure to high oxygen concentration lengthens the life span. This is considered to be the result of an increase in antioxidant defense induced by short-term oxidative stress. Mutations in genes such as age-1 and daf-2 that compose the insulin-like signaling network conferred oxidative stress resistance and an increase in Mn-SOD gene expression as well as life span extension.
衰老的自由基理论认为，氧化应激是生物体寿命的决定因素之一。在秀丽隐杆线虫中，基因或环境变化已被证明可调节寿命。在此，我们讨论自由基的产生和破坏的变化是否与这些寿命调节有关。被认为反映自由基产生的培养氧气浓度变化会扰乱寿命。高氧和低氧浓度下的寿命分别比常氧条件下的寿命短和长。短期暴露于高氧浓度会延长寿命。这被认为是短期氧化应激诱导的抗氧化防御增加的结果。组成胰岛素样信号网络的age-1和daf-2等基因的突变赋予了氧化应激抗性，增加了Mn-SOD基因表达，并延长了寿命。
